Behavioral, physiological, and genetic drivers of coping in a non-human primate.

Animals experience stressful situations, from predation to social conflicts, but mostly deal with them successfully. This adaptive mechanism, coping, reduces the adverse effects of stressors, and its failure may result in reduced fitness. Substantial inter-individual variation in coping is observed, yet little is known about how behavioral, physiological and genetic drivers regulate coping holistically and contribute to such variations. We assessed behavioral coping styles (n=30), emotional arousal (n=12), and personalities (n=32) of long-tailed macaques (Macaca fascicularis) and also investigated the association of coping with a valine/methionine polymorphism encoded by a critical human stress regulatory gene, catechol-O-methyltransferase (COMT) (n=26). Personality and the human equivalent COMT Val/Met polymorphism were associated with "nonaggression-based" and "aggression-based" coping styles. Compared to nonaggression-based, aggression-based copers maintained higher average facial temperatures, indicating potentially lower emotional arousal, as measured using infrared thermography. These findings demonstrate a complex interplay of various proximate mechanisms governing coping in a non-human primate.

Fgf3 is crucial for the generation of monoaminergic cerebrospinal fluid contacting cells in zebrafish.

In most vertebrates, including zebrafish, the hypothalamic serotonergic cerebrospinal fluid-contacting (CSF-c) cells constitute a prominent population. In contrast to the hindbrain serotonergic neurons, little is known about the development and function of these cells. Here, we identify fibroblast growth factor (Fgf)3 as the main Fgf ligand controlling the ontogeny of serotonergic CSF-c cells. We show that fgf3 positively regulates the number of serotonergic CSF-c cells, as well as a subset of dopaminergic and neuroendocrine cells in the posterior hypothalamus via control of proliferation and cell survival. Further, expression of the ETS-domain transcription factor etv5b is downregulated after fgf3 impairment. Previous findings identified etv5b as critical for the proliferation of serotonergic progenitors in the hypothalamus, and therefore we now suggest that Fgf3 acts via etv5b during early development to ultimately control the number of mature serotonergic CSF-c cells. Moreover, our analysis of the developing hypothalamic transcriptome shows that the expression of fgf3 is upregulated upon fgf3 loss-of-function, suggesting activation of a self-compensatory mechanism. Together, these results highlight Fgf3 in a novel context as part of a signalling pathway of critical importance for hypothalamic development.